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ULBP2 Antibody (Center)
Affinity Purified Rabbit Polyclonal Antibody (Pab)
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
Application 
| WB, E |
|---|---|
| Primary Accession | Q9BZM5 |
| Other Accession | NP_079493.1 |
| Reactivity | Human |
| Host | Rabbit |
| Clonality | Polyclonal |
| Isotype | Rabbit IgG |
| Calculated MW | 27368 Da |
| Antigen Region | 88-116 aa |
| Gene ID | 80328 |
|---|---|
| Other Names | NKG2D ligand 2, N2DL-2, NKG2DL2, ALCAN-alpha, Retinoic acid early transcript 1H, UL16-binding protein 2, ULBP2, N2DL2, RAET1H |
| Target/Specificity | This ULBP2 antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 88-116 amino acids from the Central region of human ULBP2. |
| Dilution | WB~~1:1000 |
| Format | Purified polyclonal antibody supplied in PBS with 0.09% (W/V) sodium azide. This antibody is purified through a protein A column, followed by peptide affinity purification. |
| Storage | Maintain refrigerated at 2-8°C for up to 2 weeks. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles. |
| Precautions | ULBP2 Antibody (Center) is for research use only and not for use in diagnostic or therapeutic procedures. |
| Name | ULBP2 |
|---|---|
| Synonyms | N2DL2, RAET1H |
| Function | Binds and activates the KLRK1/NKG2D receptor, mediating natural killer cell cytotoxicity. |
| Cellular Location | Cell membrane; Lipid-anchor, GPI-anchor. Endoplasmic reticulum. Secreted. Note=In CMV-infected fibroblasts, detected in the endoplasmic reticulum/cis-Golgi |
| Tissue Location | Expressed in various types of cancer cell lines and in the fetus, but not in normal tissues. |
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Provided below are standard protocols that you may find useful for product applications.
Background
Ligand for the NKG2D receptor, together with at least ULBP1 and ULBP3. ULBPs activate multiple signaling pathways in primary NK cells, resulting in the production of cytokines and chemokines. Binding of ULBPs ligands to NKG2D induces calcium mobilization and activation of the JAK2, STAT5, ERK and PI3K kinase/Akt signal transduction pathway. In CMV infected cells, interacts with soluble CMV glycoprotein UL16. The interaction with UL16 blocked the interaction with the NKG2D receptor, providing a mechanism by which CMV infected cells might escape the immune system. UL16 also causes ULBP2 to be retained in the ER and cis-Golgi apparatus so that it does not reach the cell surface.
References
McGilvray, R.W., et al. Int. J. Cancer 127(6):1412-1420(2010)
Nuckel, H., et al. Leukemia 24(6):1152-1159(2010)
Antoun, A., et al. Hum. Immunol. 71(6):610-620(2010)
Davila, S., et al. Genes Immun. 11(3):232-238(2010)
Ward, J., et al. PLoS Pathog. 5 (10), E1000613 (2009) :
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